Term
A) what is the preganglionic NT for the SNS?
B) What is the preganglionic NT for the PSNS?
C)What is the postganglionic NT for the SNS?
D) What is the postganglionic NT for the PSNS? |
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Definition
A) acetylcholine
B)Acetylcholine
C)Norepinephrine (and some epinephrine)
D)Acetylcholine |
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Term
A) where are ganglia located for SNS?
B) where are ganglia located for PSNS? |
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Definition
A) close to spinal cord
B) close to tissue being innervated |
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Term
| T/F. All ganglionic blockers have been removed from the market? |
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Definition
| FALSE. There is still one on the market-- mecamylamine (Inversine) |
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Term
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Definition
> ganglionic blocker originally used to treat malignant HTN. Not used anymore for HTN because there are much safer and better antihypertensives out
> Used currently to treat Tourette's syndrome (under orphan drug status)
> Has also shown to be useful in treating some cocaine and nicotine addictions.
> blocks nicotinic receptors in brain and ganglia |
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Term
| Who should you not use mecamylamine (Inversine) on? |
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Definition
| Pts with history of MI, CVA, glaucoma d/t peripheral side effects |
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Term
| What is myasthenia gravis? |
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Definition
| An autoimmune disease in which the body has circulating antibodies that block the nictonic receptors of post-synaptic neuromuscular junctions, thus inhibiting the effect of acetylcholine. |
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Term
| How do neuromuscular blocking drugs affect someone with MG? |
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Definition
| They have an exaggerated effect. Also they will have a longer duration |
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Term
A) ACh binds to the ______ subunits of neuromuscular nicotinic receptors
B)where does decamethonium bind? |
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Definition
A) alpha
B) epsilon and gamma |
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Term
T/F. There are esteratic and cationic sites on the nicotinic receptor
What binds to these sites? |
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Definition
FALSE> There are esteratic and anionic sites.
Non-depolarizing NMB contain an amine (drawn to anionic site) and an ester (drawn to esteratic site) |
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Term
| How long do cisatracurium, atracurium, rocuronium and vecuronium last? |
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Definition
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Term
A) how long does mivacurium last?
B) how long does succinylcholine last?
C) How long does pancuronium last? |
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Definition
A) 12-20 mins.
B) 3-5 mins.
C) 60-90 mins. |
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Term
A) T/F. Succinylcholine is a better choice than a non-depolarizing NMB for asthmatic patients because it is not associated with histamine release.
B) Why would succinylcholine cause any problems with someone on digoxin? |
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Definition
A) FALSE. It possesses significant histamine-releasing properties from mast-cells, which can be detrimental to asthmatic patients
B) Because it raises potassium level which patients on digoxin are very sensitive to. |
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Term
| A) How are atracurium and cisatracurium metabolized? |
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Definition
| Hofmann elimination- a deamination reaction in which there is methylation of the amine to produce a quaternary amine. This amine is removed and a double bond is formed between two carbons of the remaining compound. Water goes across this double bond causing a hydrolysis reaction in which the bond is broken in two (one part receives a H+ and the other receives a OH-) making it more polar and ready for urinary excretion. |
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Term
A) who should you avoid using cisatracurium and atracurium on?
B) What patients are these drugs good for? |
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Definition
A) epileptics because of the laudanosine (metabolite with CNS excitatory activity)
B) Renal patients |
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Term
A) what type of patients should you adjust dose or maybe even avoid use of pancuronium with?
B) What agents should you use caution with in a patient that has hepatic disease? |
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Definition
A)Patients with renal disease
B) Vecuronium and rocuronium |
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Term
| What opioid should you not use in someone that has gotten cisatracurium or atracurium? |
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Definition
| meperidine (d/t possibility of additive CNS stimulant effects) |
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Term
| What 3 NMBs have histamine releasing properties? |
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Definition
succinylcholine (most)and the benzylisoquinolines
(atracurium, cisatracurium, and mivacurium) |
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Term
| Which NMB shows greatest degree of tachycardia? |
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Definition
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Term
| Describe normal neuromuscular transmission |
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Definition
Nerve cell is electronegative at rest (-90mV). When potential is made less negative, Na+ channels open--> Na+ influx--> depolarization--> next segment is depolarized--> action potential propogates.
Depolarization sensitive Ca++ channels open--> Ca++ influx causes fusion of vesicle to wall and release of ACh into synaptic cleft--> ACh binds to the 2 alpha subunits of the nicotinic cholinergic receptor on the mucle--> nicotinic receptor ion channel opens allowing influx of Na++--> depolarization--> actional potential propogates--> MUSCLE CONTRACTION |
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Term
| What is responsible for metabolism of acetylcholine (ACh)? |
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Definition
| Acetylcholinesterase hydrolyzes ACh |
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Term
| _______ muscle relaxants are nicotinic cholinergic receptor AGONISTS and _______ muscle relaxants are competitive ANTAGONISTS |
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Definition
| Depolarizing; Non-depolarizing |
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Term
| After injection of _________, but before complete paralysis, disorganized muscular activity may occur called ________. |
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Definition
| Succinylcholine; fasciculations |
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Term
| Do cholinesterase inhibitors Potentiate or inhibit DEPOLARIZING blockade? Explain. |
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Definition
They potentiate it by 2 mechanisms:
1. By inhibiting AChE, they allow for high ACh concentration at the nerve terminal, which intensifies depolarization.
2. They reduce hydrolysis of succinylcholine by pseudocholinesterase |
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Term
| What happens when very high doses of succinylcholine are given? |
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Definition
| They can cause a desired phase I block (depolarizing) to progress to a phase II block, which resembles a Non-depolarizing block |
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Term
SUCCINYLCHOLINE
A) Dose
B) Onset
C) Duration |
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Definition
A) 1-1.5 mg/kg
B) 30-60 sec.
C) 10 mins. |
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Term
| What are the Cardiovascular side effects of Succinylcholine? |
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Definition
Since Sux is basically two ACh molecules linked together it effects all ACh receptors.
Low doses may cause sinus brady (muscarinic receptors of SA node)
High doses usually increase chronotropy and inotropy.
**Children are particularly susceptible to profound bradycardia**
Atropine is usually given prophylactically to children before the first dose of Sux and ALWAYS before a second dose. |
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Term
| How can fasciculations from Sux administration be negated? |
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Definition
| Pretreatment with a small dose (10% of intubating dose) of Non-depol. NMB about 3-5 mins. before Sux is given |
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Term
| Discuss the effect of succinylcholine on serum potassium levels. |
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Definition
Sux raises K+ levels about 0.5 mEq/L
People with denervation injuries, muscle trauma/inflammation, immobilization, and extensive burns get an UP-REGULATION of ACh receptors and therefore an EXAGGERATED hyperkalemic response to depolarizing blockade. DO NOT GIVE SUX TO THESE PATIENTS |
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Term
| Other than, CV side effects, fasciculations, and kyperkalemia, What side effects can Succinylcholine administration cause? |
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Definition
1. Elevated Intragastric pressure (this is offset by and increase in LES tone)
2. increased IOP (avoid in open eye injuries)
3. Histamine release
4. Increase in ICP (can be attenuated by precurarization)
5. MALIGNANT HYPERTHERMIA |
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Term
| How do non-depolarizing muscle relaxants work? |
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Definition
| They bind to nicotinic cholinergic receptors at the motor end plate and competitively antagonize the binding of ACh |
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Term
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Definition
| group of NDNMB's that end in -curium and tend to release histamine |
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Term
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Definition
| group of NDNMBs that end in -ronium and tend to be vagolytic |
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Term
| How do inhalational anesthetics affect NDNMB's? |
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Definition
| They decrease dosage of muscle relaxant necessary by ~15-20% |
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Term
| What can be done to ameliorate the histamine release assoc. with administration of benzylisoquinolines? |
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Definition
| Use minimum dose necessary, inject slower, and pretreat with H1 and H2 blocker |
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Term
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Definition
1. Structure- monoquaternary steroid analogue of vecuronium
2. Dosage- comes in 10 mg/mL vials intubation= 0.6-1.2 mg/kg; maintenance= 0.15mg/kg
3. Timing: onset= 60-90 secs; duration= about 60 min for 1mg/kg bolus
4. Metabolism & Excretion: Does not undergo metabolism and is eliminated primarily by liver and slightly by kidneys |
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Term
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Definition
1. STRUCTURE: pancuronium minus a quaternary methyl group--> makes it have less side effects
2. DOSAGE: comes in 10 or 20mg powder for injection
intubation= 0.08-0.12 mg/kg
maintenance= 0.01 mg/kg q15-20 min.
TIMING: onset= 2-3 mins; duration=30-45 mins.
METABOLISM & EXCRETION: metabolized slightly by liver. Depends primarily on biliary excretion. Some renal elimination |
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Term
| What are the side effects of rocuronium and vecuronium? |
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Definition
| They don't really have any major side effects. |
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Term
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Definition
1. STRUCTURE: Steroid ring with 2 modified ACh molecules (bisquarternary relaxant)
2. DOSAGE:
intubation= 0.08-0.12 mg/kg bolus
maintenance= 0.01 mg/kg Q20-40 min.
3. TIMING: onset= 2-3 min; duration= 90 mins.
4. METABOLISM & EXCRETION: limited metabolization by liver; 40% excretion by kidney and about 10% by bile |
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Term
| What are the side effects of pancuronium? |
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Definition
The most common side effect is tachycardia and hypertension**
AVOID IN PATIENTS WITH CAD AND HYPERTROPHIC CARDIOMYOPATHY |
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